AaHII

Alpha toxins bind voltage-independently at site-3 of sodium channels (Nav) and inhibit the inactivation of the activated channels, thereby blocking neuronal transmission. The toxin principally slows the inactivation process of TTX-sensitive sodium channels. It is active on rat brain Nav1.2/SCN2A sodium channel (EC(50)=2.6 nM) and on rat skeletal muscle Nav1.4/SCN4A sodium channel (EC(50)=2.2 nM) , as well as on human neuronal Nav1.7/SCN9A (EC(50)=6.8 nM). This toxin is active against mammals. In vivo, intraplantar injection into mice induces spontaneous pain responses.